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[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Differential sensitivity to 2-deoxy-D-glucose between two pancreaticcell lines correlates with GLUT-1 expression.

OBJECTIVES: To determine whether the differential growth inhibition of pancreatictumorcells to the glycolytic inhibitor 2-deoxy-D-glucose (2-DG) correlates with uptake, expression of GLUT-1 transporter, and levels of hypoxic-inducible factor-1alpha.

METHODS: Growth inhibition assays with 2-DG, lactic acid analysis, Western blots of GLUT-1, and hypoxic-inducible factor-1alpha were correlated with each other and with uptake and accumulation of radio-labeled 2-DG in 2 pancreaticcell lines.

RESULTS: Under normal oxygen tension, we find that the pancreaticcell line MIA PaCa2 (1420) is 7 times more sensitive to 2-DG and equally sensitive to oxamate, as compared with Panc-1 (1469).

Lactate levels in both cell types are similarly low, indicating that mitochondria are functioning normally in these cells and that they are not solely dependent on glycolysis for survival under an aerobic microenvironment.

Since oxamate does not use glucose transporters for entry into the cell, the equal sensitivity to this drug suggests that the selective growth inhibition of 2-DG in these 2 cell types might be reflective of differential expression of glucose transporters.

Indeed, we find that GLUT-1 is more highly expressed in 1420 and that this cell line accumulates 2-DG twice as much as 1469.

Additionally, hypoxic-inducible factor, which is known to upregulate the expression of GLUT-1, is found at equally low levels in both cell types.

CONCLUSION: Overall, our results suggest that certain pancreatic tumors may be inherently sensitive to 2-DG, even under normal oxygen tension, due to greater intracellular accumulation of this inhibitor.

Moreover, if 2-DG shows clinical efficacy, it may be possible to predict which pancreatic tumors would be sensitive to this agent based on their GLUT-1 expression profile and their increased uptake of 2-fluoro-deoxy-D-glucose currently used to image tumors via PET scanning.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

The expression of proinflammatory cytokines (tumor necrosis factor-alpha and interleukin-6), chemokines (CXCL-1, CXCL-2, and CXCL-10), and toll-like receptor 4 was significantly reduced in the treatment group, along with diminished apoptosis through caspase-3 pathway.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

The objective of this study was to investigate the function of heat shock protein 60 (HSP60) on pancreatic tissues by applying HSP60 small interfering RNA (siRNA) to reduce HSP60 expression.

Rat pancreas was isolated and pancreatic tissue snips were prepared, cultured, and stimulated with low and high concentrations of cerulein (10(-11) and 10(-5) mol/L) or lipopolysaccharide (LPS, 10 and 20 μg/mL).

Before the stimulation and 1 and 4 h after the stimulation, the viability and the level of trypsinogen activation peptide (TAP) in the tissue fragments were determined and the levels of tumor necrosis factor-alpha (TNF-α) and interleukin 6 (IL-6) in the culture supernatants were measured.

The pancreatic tissues in the control (mock-interfering) group showed a decreased viability to varying degrees after being stimulated with cerulein or LPS, and the levels of TAP, TNF-α, and IL-6 increased significantly (p < 0.05) in the tissues and/or in the culture supernatant.

The results indicated that both cerulein and LPS can induce injuries on isolated pancreatic tissues, but the induction effects are dependent on the duration of the stimulation and on the concentrations of the toxicants.

HSP60 siRNA reduces HSP60 expression and worsens the cerulein- or LPS-induced injuries on isolated pancreatic tissues, suggesting that HSP60 has a protective effect on pancreatic tissues against these toxicants.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Gli1 promotes cell survival and is predictive of a poor outcome in ERalpha-negative breast cancer.

Gli1 is a transcription factor and oncogene with documented roles in the progression of several cancer types, including cancers of the skin and pancreas.

In order to investigate the functional impact of Gli1 in breast cancer, expression of Gli1 and its contribution to cell growth was assessed in breast cancer cell lines.

In these cancers, the association of Gli1 with expression of estrogen receptor alpha (ERalpha) and progesterone receptor (PR), ErbB2, p53, the rate of proliferation, and clinicopathologic parameters and outcome was assessed.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

In overweight children and adults, low plasma SHBG levels are a biomarker of the metabolic syndrome and its associated pathologies.

Here, we showed in transgenic mice and HepG2 hepatoblastoma cells that monosaccharides (glucose and fructose) reduce human SHBG production by hepatocytes.

The dose-dependent reduction of HNF-4alpha levels in HepG2 cells after treatment with glucose or fructose occurred in concert with parallel increases in cellular palmitate levels and could be mimicked by treatment with palmitoyl-CoA.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Regulation and functional role of the Runt-related transcription factor-2 in pancreatic cancer.

In the present study, the localisation of the Runt-related transcription factor-2 (Runx2), its transcriptional activity, as well as its regulation of expression was analysed in human pancreatic ductal adenocarcinoma (PDAC).

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Tauhe expression of the critical initiator cytokine TNF-alpha was strongly upregulated in vivo in acute necrotic pancreatitis (AP) in rodents and in vitro in TNF-alpha activated acinar AR42J cells.

Upregulation of tnf-alpha, inos, icam-1 and il-6 occurred both in TNF-alpha receptor 1 and 2 knock-out mice, but not in TNF-alpha knock-out mice, in cerulein-induced acute pancreatitis.

Activation of tnf-alpha gene was also accompanied by an ordered increased level of histone H3K9, H3K14 and H3K18-acetylation and H3K4 methylation, as well as H4K5 acetylation.

A better knowledge of the molecular mechanisms that control tnf-alpha gene regulation will provide deeper understanding of the initiation and development of the inflammatory processes occurring in acute pancreatitis triggered by TNF-alpha cytokine.

[Title] Protein kinase C: a target for therapy in pancreatic cancer.

This study investigated the expression of PKC in pancreatictumor tissue in comparison to adjacent normal tissue and determined the modulation of PKC by bryostatin-1 (BRYO) on pancreatic cancer cell lines.

METHODS: Pancreatic tissue was obtained from 18 patients who had a resection (14 with ductal adenocarcinoma and 4 with adenoma and high-grade dysplasia).

HPAC cells were treated with gemcitabine and BRYO and in sequential and concomitant combination.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Histopathological examination of ultrasound-guided needle biopsy from a hepatic lesion demonstrated a neuroendocrinetumor.

Somatostatin-receptor scintigraphy with radio-labelled octreotide confirmed the likelihood of the neuroendocrine nature of the hepatic tumors and excluded the presence of other such lesions throughout the rest of the body, including the pancreas.

The serum glucagon level was markedly increased.

The diagnosis of necrolytic migratory erythema associated with hyperglucagonemia and neuroendocrine hepatic tumors was made and therapy with the long-acting somatostatin analogue octreotide was started.

Having reached the final stage of the disease, which was further complicated by congestive heart failure, the patient died one year later.

As no autopsy was performed, we were unable to establish whether the hepatic tumors represented a metastatic process of previously undetected pancreatic glucagonoma or if they were extra-pancreatic glucagon-secreting tumors.

The correct diagnosis of necrolytic migratory erythema is important, since it might be the clue for early detection of glucagonoma or of extra-pancreatic glucagon-secreting tumors.

The levels of BDNF in synovial tissue were not correlated with the number of inflammatory cells observed microscopically or with levels of TNFalpha.

However, the levels of BDNF in plasma of patients treated with anti-TNF did not correlate with the changes in ESR or a disease activity score.

Instead it is likely that sources other than inflammatory cells, including nerve structures, are important sources of BDNF and that the effects of anti-TNF treatment on BDNF levels may be related to effects on circulating and various local cells and/or BDNF-containing neurons.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Calcium phosphate cement chamber as an immunoisolative device for bioartificial pancreas: in vitro and preliminary in vivo study.

OBJECTIVES: This study examined a calcium phosphate cement (CPC) chamber as an immunoisolative device to facilitate the use of xenogeneic cell sources without immunosuppression for the bioartificial pancreas (BAP).

METHODS: Mouse insulinoma cells were encapsulated in agarose gel and then enclosed in a CPC chamber to create a BAP.

Bioartificial pancreas were evaluated by cell viability, live-dead cell ratio, and cytokine-mediated cytotoxicity assay and implanted into the peritoneal cavity of diabetic rats.

RESULTS: Insulinoma cells enclosed in the CPC chamber had normal viability, cell survival, and insulin secretion that was even cultured in media with cytokines.

Histological examination revealed the fibrous tissue envelopment, and immune-related cells that competed for oxygen resulting in hypoxia could be attributed to the dysfunction of BAPs.

An alternative implanted site should be considered to extend the functional longevity of BAPs in further study.

[Other-IDs] NLM/ PMC1569868

24. Steiner AA, Romanovsky AA: Leptin: at the crossroads of energy balance and systemic inflammation.Prog Lipid Res; 2007 Mar;46(2):89-107[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

In leptin-irresponsive mutants, the hypothermia of systemic inflammation is exaggerated, presumably due to the enhanced production and cryogenic action of tumor necrosis factor (TNF)-alpha.

The enhanced production of TNF-alpha and IL-1beta may be due, at least in part, to insufficient activation of the anti-inflammatory hypothalamo-pituitary-adrenal axis by immune stimuli in the absence of leptin signaling.

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[Publication-country] England

[Chemical-registry-number] 0 / Leptin; 0 / Receptors, Leptin

[Number-of-references] 209

[Other-IDs] NLM/ NIHMS23764; NLM/ PMC1976277

25. de Herder WW: Biochemistry of neuroendocrine tumours.Best Pract Res Clin Endocrinol Metab; 2007 Mar;21(1):33-41[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Biochemistry of neuroendocrine tumours.

Several circulating or urinary tumour markers can be used for the diagnosis and follow-up of functioning and clinically non-functioning neuroendocrine tumours of the pancreatic islet cells and intestinal tract.

Among the specific tumour markers are serotonin and its metabolites--e.g.

5-hydroxyindoleacetic acid (5-HIAA)--in carcinoid tumours and the carcinoid syndrome, insulin and its precursors or breakdown products in insulinoma, and gastrin in gastrinoma.

Plasma vasointestinal polypeptide (VIP) determinations have been used in the diagnosis of VIPoma, plasma glucagon for glucagonoma, and serum somatostatin for somatostatinoma.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

BACKGROUND: Pancreatic cancer is a complex genetic disorder that is characterized by rapid progression, invasiveness, resistance to treatment and high molecular heterogeneity.

Various agents have been used in clinical trials showing only modest improvements with respect to gemcitabine-based chemotherapy, which continues to be the standard first-line treatment for this disease.

However, owing to the overwhelming molecular alterations that have been reported in pancreatic cancer, there is increasing focus on targeting molecular pathways and networks, rather than individual genes or gene-products with a combination of novel chemotherapeutic agents.

The CK2 protein expression levels were determined and the effect of its down-regulation on chemosensitization of pancreatic cancer cells was investigated.

RESULTS: The present study examined the impact on cell death following depletion of the individual protein kinase CK2 catalytic subunits alone or in combination with gemcitabine and the molecular mechanisms by which this effect is achieved.

Depletion of the CK2alpha or -alpha' subunits in combination with gemcitabine resulted in marked apoptotic and necrotic cell death in PANC-1 cells.

We show that the mechanism of cell death is associated with deregulation of distinct survival signaling pathways.

CONCLUSIONS: Results reported here show that the two catalytic subunits of CK2 contribute differently to enhance gemcitabine-induced cell death, the reduced level of CK2alpha' being the most effective and that simultaneous reduction in the expression of CK2 and other survival factors might be an effective therapeutic strategy for enhancing the sensitivity of human pancreatic cancer towards chemotherapeutic agents.

METHODOLOGY: To assess if the mutations are present in other tumor types we performed a systematic mutational profile of the GNAQ exon 5 in a panel of 922 neoplasms, including glioblastoma, gastrointestinal stromal tumors (GIST), acute myeloid leukemia (AML), blue naevi, skin melanoma, bladder, breast, colorectal, lung, ovarian, pancreas, and thyroid carcinomas.

Changes affecting Q209 were not found in any of the other tumors.

Our data indicate that the occurrence of GNAQ mutations display a unique pattern being present in a subset of melanocytic tumors but not in malignancies of glial, epithelial and stromal origin analyzed in this study.

[Other-IDs] NLM/ PMC2730032

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] EUS-Guided Antitumor Therapy for Pancreatic Tumors.

Endoscopic ultrasound (EUS) is a very useful modality for the diagnosis and staging of pancreatic masses.

With the advent of EUS-guided fine-needle aspiration technology, this modality has made a tremendous leap from imaging modality to histologic diagnosis and therapeutic intervention.

EUS offers high-resolution images of and unparalleled access to the pancreas.

After locating the tip of the echoendoscope in the duodenum or stomach, several drugs or local treatment modalities can be delivered directly into the pancreas.

EUS-guided ethanol lavage with/without paclitaxel injection has been tested for the treatment of cystic tumors of the pancreas, with complete resolution of cystic tumor being observed in up to 70-80% of patients.

Ethanol injection is also performed for the management of solid neuroendocrine tumors of the pancreas.

Various type of EUS-guided injection have also been investigated for the treatment of pancreatic cancer.

A replication-deficient adenovirus vector carrying the tumor necrosis factor-alpha gene was also delivered intratumorally by EUS.

ONYX-015 is an oncolytic attenuated adenovirus that exhibits replication preferentially in malignant cells, causing cell death, and this has also been injected into pancreatic cancers under EUS guidance.

This article reviews the various applications of EUS for the treatment of pancreatic tumors.

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[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

BACKGROUND: In patients suffering from acute pancreatitis, the pathogenesis is not completely understood, and several recent studies in vitro suggested that heat shock proteins might play an important role in cell signaling.

CONCLUSIONS: The results suggest that extracellular Hsp70 might induce systemic inflammatory response syndrome (SIRS)-like response in vivo and TLR4 might be involved in the Hsp70-mediated activation of inflammatory reaction in the progression of CIP without infection.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Multiple endocrine neoplasia type 1 deletion in pancreaticalpha-cells leads to development of insulinomas in mice.

The pancreaticalpha- and beta-cells are critical components in regulating blood glucose homeostasis via secretion of glucagon and insulin, respectively.

Both cell types are typically localized in the islets of Langerhans.

The lack of suitable cell lines to study alpha- and beta-cells interactions have led us to develop an alpha-cell-specific Cre-expressing transgenic line utilizing a glucagon promoter sequence, the Glu-Cre transgenic mouse.

Here, we demonstrate that the Glu-Cre could specifically and efficiently excise floxed target genes in adult isletalpha-cells.

We further showed that deletion of the tumor suppressor gene, multiple endocrine neoplasia type 1 (Men1), in alpha-cells led to tumorigenesis.

However, to our surprise, the lack of Men1 in alpha-cells did not result in glucagonomas but rather beta-cell insulinomas.

Because deletion of the Men1 alleles was only present in alpha-cells, our data suggested that cross communication between alpha- and beta-cells contributes to tumorigenesis in the absence of Men1.

Together, we believed that the new model systems described here will allow future studies to decipher cellular interactions between isletalpha- and beta-cells in a physiological context.

[ISO-abbreviation] Endocrine

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

36. Patel M, Fine DR: Fibrogenesis in the pancreas after acinar cell injury.Scand J Surg; 2005;94(2):108-11[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Fibrogenesis in the pancreas after acinar cell injury.

Fibrosis within the pancreas is a key feature of chronic pancreatitis and pancreatic cancer.

It has now been well demonstrated that following injury to acinar cells, pancreatic stellate cell activation, migration and proliferation is the key mediator of this process.

The pancreatic stellate cell is likely to play an important role in maintaining the normal extracellular matrix; we speculate that the dysregulation of this process is an important factor in chronic pancreatitis.

[Number-of-references] 22

37. Santini D, Poli F, Lega S: Solid-papillary tumors of the pancreas: histopathology.JOP; 2006;7(1):131-6[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Solid-papillary tumors of the pancreas: histopathology.

A solid-pseudopapillary tumor is an uncommon and "enigmatic" pancreatic neoplasm, and the term encompasses the two most conspicuous histological features: solid and pseudopapillary areas.

Histologically, solid-pseudopapillary tumors are generally characterized by solid areas alternating with a pseudopapillary pattern, and cystic spaces which are the results of degenerative changes occurring in the solid neoplasm.

Its immunohistochemical pattern is very distinctive and neoplastic cells are consistently vimentin-, CD10- and CD56-positive.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

We studied the consequences of this drug on antithrombin levels, activity, conformation, and immunohistological and ultrastructural features in plasma from acute lymphoblastic leukemia patients, HepG2 cells, and plasma and livers from mice treated with this drug.

Similar effects were observed for alpha1-antitrypsin in plasma, cells, and livers, and intracellular aggregates of additional proteins were observed in frontal cortex and pancreas.

This is the first report of a conformational drug-associated effect on serpins without genetic factors involved. l-Asparaginase treatment induces severe, acquired, and transient type I deficiency of antithrombin (and alpha1-antitrypsin) with intracellular accumulation of the nascent molecule, increasing the risk of thrombosis.

Western blotting analysis revealed significant elevation of ceruloplasmin, complement C3, afamin, and alpha-1-B-glycoprotein in the plasma of SCC patients in comparison to controls.

Immunoturbidimetric assay of a larger group confirmed the results of 2-DE and Western blotting, and showed that ceruloplasmin and complement C3 were significantly elevated in the plasma of SCC patients in comparison with controls and patients with carcinoma in situ (CIS) of the uterine cervix.

CONCLUSION: Plasma protein expression determined using 2-DE and MALDI-MS will give a chance to identify tumor-specific biomarkers for SCC of the cervix.

[Publication-type] Journal Article

[Publication-country] Korea (South)

[Other-IDs] NLM/ PMC2676467

47. Chamson-Reig A, Arany EJ, Summers K, Hill DJ: A low protein diet in early life delays the onset of diabetes in the non-obese diabetic mouse.J Endocrinol; 2009 May;201(2):231-9[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Dietary insult in early life can affect the development and future function of the endocrine pancreas.

Serum insulin and pancreatic insulin content were reduced in LP-fed NOD offspring at 8 weeks, as were serum interferon gamma and pancreatictumor necrosis factor alpha, while the number of pancreatic islets demonstrating peri-insulitis, and the degree of invasiveness were reduced.

To determine if LP caused early morphometric changes in the pancreas, we measured mean islet area at days 3 and 21.

Mean islet size did not differ with diet, but by 8 weeks of age LP-fed NOD females exhibited a significantly reduced islet number and mean islet area, and a lower fractional area of pancreas occupied by both alpha- and beta-cells than control-fed mice.

The mechanism is likely to involve both altered beta-cell morphology and function and changes in cytotoxic cytokines.

In the present studies, we investigated whether insulin-induced HIF-1alpha expression is a prerequisite for insulin to induce other trophic effects in MiaPaCa2 human pancreatic cancer cells and whether inhibition of HIF-1alpha expression would decrease tumor glycolysis and improve host energy homeostasis.

We found that hypoxia was a prerequisite for induction of HIF-1alpha mRNA expression by insulin in MiaPaCa2 cells.

Under hypoxic conditions, insulin stimulated glycolysis, cell proliferation, and the secretion of vascular endothelial growth factor in regular MiaPaCa2 cells but not in a MiaPaCa2 variant (si-MiaPaCa2) that expressed specific short interfering RNA for HIF-1alpha and therefore lacked HIF-1alpha protein.

When si-MiaPaCa2 cells were transplanted into the pancreas of athymic mice, they were less tumorigenic and expressed less hexokinase than regular MiaPaCa2 cells.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

BACKGROUND & AIMS: Pancreatic stellate cells have been characterized as the major source of extracellular matrix and cytokine production in the pancreas.

This study showed that pancreatic stellate cells have a phagocytic function.

METHODS: The morphological features of periacinar phagocytic cells were investigated by immunohistochemically staining serial sections of the pancreas from male WBN/Kob rats and an animal model of acute pancreatitis for glial fibrillary acidic protein and alpha-smooth muscle actin.

Pancreatic stellate cells were assayed for phagocytic activity by incubating them with senescent polymorphonuclear neutrophils or fluorescence-labeled latex beads in the presence or absence of cytokines, growth factors, and peroxisome proliferator-activated receptor gamma ligand.

RESULTS: Phagocytic cells were observed in areas of inflammation, and they were identical to the glial fibrillary acidic protein-positive and alpha-smooth muscle actin-positive cells, thus suggesting that they were pancreatic stellate cells.

Aged polymorphonuclear neutrophils were ingested into the cytoplasm of the pancreatic stellate cells.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Inhibitory effect of the lectin wheat germ agglutinin (WGA) on the proliferation of AR42J cells.

The rat pancreatic acinar tumourcell line AR42J is a widely used model to study the secretion, proliferation and differentiation of cells under the influence of hormones.

These so-called amphicrine cells synthesize and secrete digestive enzymes as well as neuroendocrine peptides.

They possess both subtypes of the highly glycosylated cholecystokinin (CCK) receptor which are important for the regulation of secretion and for cell growth.

AR42J cells extrude CCK and gastrin-like hormone peptides and have the ability of an autostimulation (autocrine loop).

The lectins wheat germ agglutinin (WGA) and Ulex europaeus agglutinin (UEA-I) bind to the glycosylated sites of these CCK receptors with the effect inhibiting CCK binding and thus inhibiting the CCK-induced Ca2+ release and alpha-amylase secretion.

The so-called trophic hormones CCK and gastrin stimulate the secretion and proliferation of AR42J cells within the autocrine loop via autostimulation of their CCK receptors.

In preceding papers, we described the inhibitory effect of WGA on the binding of 125I-CCK-8s to the CCK-A and -B receptors and the subsequent enzyme secretion of AR42J cells.

In the present work, we studied the influence of the lectins WGA, UEA-I and galectin-1, as well as of the lectin-like enzyme alpha-amylase, on the proliferation of AR42J cells and prevention of autostimulation.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Characterization and role of fucose mutarotase in mammalian cells.

Based on sequence comparison of mouse and human homologs with the prokaryotic fucose mutarotases (FucU) characterized previously, we investigated their function in mammalian cells.

The mouse gene was widely expressed in various tissues and cell lines, including kidney, liver, and pancreas, although expression was marginal in muscle and testis.

By generating stably expressed cell lines for mutarotase genes in HepG2, it was shown that fucose incorporations into cellular proteins were increased as demonstrated by an incorporation of radiolabeled fucose into the cells.

[Publication-country] England

53. Shi Y, Sahu RP, Srivastava SK: Triphala inhibits both in vitro and in vivo xenograft growth of pancreatic tumor cells by inducing apoptosis.BMC Cancer; 2008;8:294[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Triphala inhibits both in vitro and in vivo xenograft growth of pancreatictumorcells by inducing apoptosis.

This study elucidates the molecular mechanism of Triphala against human pancreatic cancer in the cellular and in vivo model.

METHODS: Growth-inhibitory effects of Triphala were evaluated in Capan-2, BxPC-3 and HPDE-6 cells by Sulphoradamine-B assay.

Apoptosis was determined by cell death assay and western blotting.

Tumors were analyzed by immunohistochemistry and western blotting.

RESULTS: Exposure of Capan-2 cells to the aqueous extract of Triphala for 24 h resulted in the significant decrease in the survival of cells in a dose-dependent manner with an IC50 of about 50 microg/ml.

Triphala-mediated reduced cell survival correlated with induction of apoptosis, which was associated with reactive oxygen species (ROS) generation.

Triphala-induced apoptosis was linked with phosphorylation of p53 at Ser-15 and ERK at Thr-202/Tyr-204 in Capan-2 cells.

Above mentioned effects were significantly blocked when the cells were pretreated with an antioxidant N-acetylcysteine (NAC), suggesting the involvement of ROS generation.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Effects of alpha-adrenoreceptor antagonists on apoptosis and proliferation of pancreatic cancer cells in vitro.

AIM: To discuss the expression of alpha-adrenoreceptors in pancreatic cancer cell lines PC-2 and PC-3 and the effects of alpha1- and alpha2-adrenoreceptor antagonists, yohimbine and urapidil hydrochloride, on the cell lines in vitro.

However, exposure to urapidil hydrochloride increased DNA synthesis in PC-2 cell lines as compared to the control group.

PC-2 cell lines were sensitive to both drugs.

The proliferation of the 2 cell lines was inhibited by yohimbine.

CONCLUSION: The expression of alpha1- and alpha2-adrenoreceptors is different in PC-2 and PC-3 cell lines, which might be indicative of their different functions.

The alpha2-adrenoceptor antagonist, yohimbine, can inhibit the proliferation of both cell lines and induce their apoptosis, suggesting that yohimbine can be used as an anticancer drug for apoptosis of PC-2 and PC-3 cells.

A patient who survived for 21 years since initial discovery of glucagonoma with concurrent liver metastases is described.

The longevity of this patient may be related to the slow tumor growth expressed histologically by ischemic necrosis of the malignant cells and in imaging by extensive tumor calcifications, a very rare finding in this type of the tumor.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

The use of radiolabeled antibodies that are able to target primary tumors as well as metastatic tumor sites with minimal reactivity to normal tissues is a promising approach for treating pancreatic cancer.

In this study, the integrin alpha(v)beta(5) is studied as a target for the diagnosis of and potential therapy for human pancreatic cancer by using the radiolabeled murine monoclonal antibody (mAb) 14C5.

Biopsy specimens from human pancreatic tumors were examined for the expression of the integrin alpha(v)beta(5).

The pancreatictumor cell line Capan-1 was used to test the in vitro targeting potency of mAb 14C5 labeled with 125/131-iodine and 111-indium.

Biodistribution and tumor-targeting characteristics were studied in Capan-1 xenografts.

All tumor sections were positive for the integrin alpha(v)beta(5), with an extensive positive staining of the stroma.

Planar gamma imaging with mAb 14C5 indicated clear localization of the pancreatic tumors versus minimal normal tissue uptake. mAb 14C5 is a promising new antibody for targeting the integrin alpha(v)beta(5) for the diagnosis of and potential therapy for pancreatic cancer.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

Multivisceral surgical resection for cure was successfully performed in a 70-year-old man suffering from a primary hepatocellular carcinoma (HCC) associated with direct invasion to the stomach and pancreas.

The patient presented with gastric outlet obstruction, upper abdominal pain and a history of chronic liver disease due to hepatitis B virus (HBV) infection.

At 2 days post-cancer cell subcutaneous inoculation, mice were injected with AC by local or systemic injection.

The AC can target and kill cancer cells in vitro in a concentration-dependent fashion.

Some 90% of TUNEL positive cells were found after incubation with 1.2 MBq/ml of AC.

A single local injection of approximately 222 MBq/kg 2 days post-cell inoculation can completely inhibit tumor growth over 12 weeks, and an intraperitoneal injection of 111 MBq/kg causes significant tumor growth delay.

CONCLUSIONS: (213)Bi-PAI2 can specifically target pancreatic cancer cells in vitro and inhibit tumor growth in vivo. (213)Bi-PAI2 may be a useful agent for the treatment of post-surgical pancreatic cancer patients with minimum residual disease.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

OBJECTIVE: Hypoxia-inducible factor 1alpha (HIF-1alpha) has been universally detected in many types of cells and plays a key role in modulation of tumor-related genes.

The purpose of this study was to explore the relationship between HIF-1alpha messenger RNA (mRNA) expression and biologic characteristics in pancreatic cancer, such as tumor angiogenesis, tumor cell proliferation, differentiation, apoptosis, and metastasis.

RESULTS: There was very significant difference in the expression of HIF-1alpha between the pancreatic cancer tissue and adjacent normal tissue (P < 0.01), but no significant difference was found among tumor histopathologic grades (P > 0.05).

There was significant difference in the expression of HIF-1alpha mRNA between Japanese Pancreatic Society stages I to II and stages III to IV (P < 0.05).

CONCLUSION: The expression level of HIF-1alpha mRNA is surmised to have a significant correlation with tumor angiogenesis, cell proliferation, apoptosis, and metastasis.

Inhibition of HIF-1alpha may be an important and approachable therapeutic target for pancreatic cancer.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] [Effects of Chaiqin Chengqi Decoction on activation of nuclear factor-kappaB in pancreas of rats with acute necrotizing pancreatitis].

Blood sample was collected from abdominal vein for examination and the pancreatic tissue samples were taken for making pathology section 6 hours later.

The pancreatic tissue (HE staining) was observed by light microscope.

The content of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) was detected with the method of enzyme-linked immunosorbent assay, and the activation of nuclear factor-kappaB (NF-kappaB) in pancreas was detected by immunohistochemical method.

RESULTS: Compared with the SO group, there was dramatic increase in the white blood cell (WBC) counts and AMY level in the ANP group (P<0.05, P<0.01).

The integral optical density of NF-kappaB p65 positive cells ofpancreas in CQCQD-treated group was lower than that in the ANP group (P<0.05).

CONCLUSION: CQCQD can reduce the content of serum TNF-alpha and IL-6, depress the activation of NF-kappaB, and lessen the pancreatic lesions.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

The efficacies of two nutritional factors, folic acid and vitamin B12, were assessed in this study against arsenic-induced islet cellular toxicity.

Results showed that, compared to control group, there was a significant increase in the levels of nitric oxide (NO), malondialdehyde (MDA) and hydroxyl radical (OH-) formation in the pancreatic tissue of arsenic-treated rats, while the activity of antioxidant enzymes, superoxide dismutase (SOD) and catalase (CAT), and cellular content of antioxidant glutathione (GSH) were low in these animals.

The serum level of tumor necrosis factor-alpha (TNF-alpha) and IL-6 was significantly high in these animals.

Light microscopic examination showed a marked fall in the number of islet cells.

Although folic acid alone could not restore the normal level of TNF-alpha and IL-6, combined folic acid and vitamin B12 could restore it.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

BACKGROUND: A major obstacle in treatment of solid tumors is the inefficient delivery of therapeutic agents to the hypoxic cores.

Hypoxia offers the potential for anaerobic bacteria colonization and tumor destruction by the bacteria, and dormant spores of wild-type Clostridium perfringens (Cp) germinate and proliferate within the hypoxic cores of pancreatic tumors in mice.

METHODS: Recombinant Cp strains in which superoxide dismutase, a major oxygen tolerance gene, was deleted (Cp/sod(-)) were constructed to enhance its selective growth in tumors.

The ability of the recombinant Cp strains to kill tumors was investigated in C57/BL6 mice bearing murine PANC02 tumors.

CONCLUSIONS: Cp/sod(-)/PVL provides a prototype for a novel class of oncopathic microbes that may have potential for the safe and effective treatment of pancreatic cancer and other poorly vascularized tumors.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title] Suppressor of cytokine signaling-1 in T cells and macrophages is critical for preventing lethal inflammation.

Here, cre/loxP deletion of Socs1 was used to investigate the contribution of specific cells/tissues to inflammatory disease.

Mice with SOCS-1 deficiency in myeloid and lymphoid cells, but not lymphoid alone, became ill at 50 to 250 days of age.

These mice developed splenomegaly and T-cell/macrophage infiltration of many organs, including liver, lung, pancreas, and muscle.

There were also abnormally high levels of the proinflammatory cytokines interferon gamma (IFN-gamma), tumor necrosis factor (TNF), and interleukin-12 (IL-12), and activated T cells circulating in these mice.

Socs1(null) T cells were found to be hypersensitive to multiple cytokines, including IL-1, IL-2, and IL-12, resulting in IFN-gamma production without requiring T-cell receptor (TCR) ligation.

A dysregulated cytokine network between T cells and macrophages is thus associated with this inflammatory disease.

These findings indicate that SOCS-1 is critical in both T cells and macrophages for preventing uncontrolled inflammation.

METHODS: In the present study, we evaluated c-Jun NH(2)-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) activation, and cytokine production, in pancreata of duct-ligated rats with and without duodenal bile-pancreatic juice replacement from a donor rat.

We hypothesized that enteral exclusion of bile-pancreatic juice activates stress kinases and induces cytokine production in ligation-induced acute pancreatitis.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

We report a case of necrolytic migratory erythema (NME) without glucagonoma associated with hepatitis B.

Although the most common cause of NME is a glucagon-secreting alpha-isletcell tumor of the pancreas, a dermatitis clinically and histologicaly identical to NME has been described in patients without glucagonoma.

We added some discussion on the terminology of this disease.

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(PMID = 15701595.001).

[ISSN] 1167-1122

[Journal-full-title] European journal of dermatology : EJD

[ISO-abbreviation] Eur J Dermatol

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] France

73. Prout TM, Taylor AJ: Case of the season: glucagonoma syndrome.Semin Roentgenol; 2005 Jan;40(1):4-7[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[MeSH-minor] Female. Humans. Middle Aged. Syndrome

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(PMID = 19317246.001).

[ISSN] 1784-3286

[Journal-full-title] Acta clinica Belgica

[ISO-abbreviation] Acta Clin Belg

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] Belgium

75. Oberg K: Pancreatic endocrine tumors.Semin Oncol; 2010 Dec;37(6):594-618[Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

[Title]Pancreatic endocrine tumors.

Pancreatic endocrine tumors have been steadily growing in incidence and prevalence during the last two decades, showing an incidence of 4-5/1,000,000 population.

They represent a heterogeneous group with very varying tumor biology and prognosis.

About half of the patients present clinical symptoms and syndromes related to substances released from the tumors (Zollinger-Ellison syndrome, insulinoma, glucagonoma, etc) and the other half are so-called nonfunctioning tumors mainly presenting with symptoms such as obstruction, jaundice, bleeding, and abdominal mass.

Ten percent to 15% of the pancreatic endocrine tumors are part of an inherited syndrome such as multiple endocrine neoplasia type 1 (MEN-1), von Hippel-Lindau (VHL), neurofibromatosis, or tuberousclerosis.

The diagnosis is based on histopathology demonstrating neuroendocrine features such as positive staining for chromogranin A and specific hormones such as gastrin, proinsulin, and glucagon.

Moreover, the biochemical diagnosis includes measurement of chromogranins A and B or specific hormones such as gastrin, insulin, glucagon, and vasoactive intestinal polypeptide (VIP) in the circulation.

Surgery is still one of the cornerstones in the management of pancreatic endocrine tumors, but curative surgery is rarely obtained in most cases because of metastatic disease.

[Other-IDs] NLM/ PMC4171226

78. Szabo G, Mandrekar P, Oak S, Mayerle J: Effect of ethanol on inflammatory responses. Implications for pancreatitis.Pancreatology; 2007;7(2-3):115-23[Fulltext service] Download fulltext PDF of this article and others, as many as you want.

[Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.

BACKGROUND/AIMS: Alcohol use alters inflammatory cell responses.

While alcohol has direct effects on pancreatic acinar cells, activation of inflammatory cells is a major component of the pathology of alcoholic pancreatitis.

Our results support the hypothesis that both acute alcohol intake in the presence of complex stimuli (such as necrotic cells) and chronic alcohol exposure result in hyper-responsiveness of monocytes to inflammatory signals and may contribute to increased inflammation in pancreatitis.